Viva 1

The rest of the viva focussed on the management of refractory ICP including a discussion of the DECRA trial results.

Stereotypical first steps in management:

• Position the head (45 °head up, facing straight)
• Loosen the ETT ties
• Remove the C-spine collar (if one was applied)
• Decrease PEEP as much as possible
• Drain the EVD (10ml)
• Maintain a low-normal PaCO₂ (35-40 mmHg)
• Increase sedation
  • Propofol sedation to decrease distress and thus decrease ICP
  • Benzodiazepines may be of use (but they do not decrease the CMRO₂ as much as propofol)
• Paralysis with neuromuscular junction blocker

The ICP improves. What other "neuroprotective" measures would you employ?

• Normoxia: keep the PaO₂ above 60 mmHg
• Normotension: measure the MAP, and keep the systolic above 90mmHg
• Intracranial Pressure monitoring: keep it under 20mmHg
• Cerebral perfusion pressure: keep it 50-70mmHg
• Cerebral oxygenation monitoring:keep the SjO₂ >50%, and PbrO₂ >55mmHg
• Managing increased intracranial pressure as above
• Analgesia - opioid selection is irrelevant, but opiate boluses increase ICP
• Seizure prophylaxis is infrequently indicated, and the course is 7 days only

What is the evidence that intracranial pressure monitoring is of benefit in TBI?

Not all studies uniformly demonstrate benefit:

• A 2012 randomised controlled trial of ICP monitoring versus imaging and clinical examination did not demonstrate superiority of one over the other in terms of mortality or functional outcome ​(Chesnut et al, 2012) 
• In 2014, a meta-analysis scraped together 11,038 patients worth of trial and cohort data, also concluding "no benefit" in the face of severe heterogeneity (Su et al, 2014)
•  Cremer et al (2005) associated ICP-guided therapy with increased intensity of therapy and more prolonged mechanical ventilatio

The BTF Guidelines recommend ICP monitoring be carried out in those patients which meet their indications:

• Anyone with an abnormal CT and GCS 3-8 gets ICP monitoring
• Anyone with a normal CT, GCS 3-8, 
  and any two of the following features:
  • Age over 40
  • Systolic BP <90
  • Motor posturing

This is on the basis of a 2015 retrospective study (Dawes et al) finding a substantial decrease in mortality (30.7% vs. 45.7%).

Recent observational data suggest that certain groups might benefit from ICP monitoring more than others. Specifically, groups which benefit in terms of mortality are as follows:

• GCS of 3-5 at admission.
• GCS of 9-12 which drops to 3-8 within 24 hours.
• Those who had a probability of death greater than 60% at 6 months.

What is your practice regarding seizure prophylaxis following TBI, and why?

• Approximately 5-7% of TBI patients experience post-traumatic seizures.
• Neurotoxicity from such seizures represents a preventable morbidity
• Seizure activity (even when non-convulsive, and in the context of a protected airway) is a cause for increased cereberal metabolic demand, and may cause secondary brain injury.
• Antiepileptic therapy is not without its risks, but uncontrolled seizures in TBI represent an even greater risk
• However, there does not seem to be any evidence that reduction in post-traumatic seizures within the first week decreases long term mortality in any way.

Own practice:

• The 2003 AAN guidelines recommend a one-week course of therapy.
• There is no evidence to support prophylaxis for longer than seven days after TBI, even if risk factors are present.

What are the risk factors for post-traumatic seizures?

This answer was taken directly from the Brain Trauma Organisation Guidelines for Management Traumatic Brain Injury. 

• Glasgow Coma Scale (GCS) Score < 10
• Cortical contusion
• Depressed skull fracture
• Subdural hematoma
• Epidural hematoma
• Intracerebral hematoma
• Penetrating head wound
• Seizure within 24 h of injury

Risk Factors for Early and Late Post-Traumatic Seizures

Risk factors for early seizures Glasgow Coma Scale score of ≤10 Immediate seizures Cortical contusion Linear fracture No or brief unconsciousness Penetrating head injury Depressed skull fracture Age ≤ 65 yr Increased severity of injury Chronic alcoholism Postraumatic amnesia lasting longer than 30 min Subdural, epidural, or intracerebral hematoma

Risk factors for late seizures Early post-traumatic seizures Acute intracerebral hematoma Cortical contusion Increased severity of injury Posttraumatic amnesia lating longer than 24 hr Loss of consciousness Age > 65 yr

What is your choice of agent for post-traumatic seizure prophylaxis, and why?

• Phenytoin has been the drug of choice. BTF were unable to find any evidence to recommend levitiracetam over phenytoin.
  • Advantages include:
    • Its cheap.
    • Its safe.
    • Its effective (at least in preventing early post-TBI seizures)
  • Disadvantages include:
    • It requires monitoring
    • The exact therapeutic level to aim for in TBI is not well established
    • It has extensive interactions
    • It has unusual nonlinear elimination kinetics
    • It may have a negative effect on long-term cognitive function

• Levitiracetam is becoming the drug of choice.
  • Advantages include:
    • Its as safe and at least as effective as phenytoin
    • It has a more benign pharmacokinetic profile
    • It does not require monitoring (but only because levels do not correlate with effect)
  • Disadvantages include:
    • Its expensive
    • There are no studies to convincingly demonstrate its superiority over phenytoin. A survey of epilepsy specialists conducted in 2015 has demonstrated that there is genuine equipoiseamong senior medical experts, to the point where one major neurotrauma center might use exclusively phenytoin, and the other might use only levitiracetam.

Own  practice:

• Pragmatically, the two agents are indistinguishable in their efficacy, but levitiracetam does not require monitoring and has lower toxicity.

The patient suddenly has a "spike" of ICP up to 44mmHg. How would you respond to this situation?

Assess again:

• Ensure monitoring is accurate
• Ensure pupils are equal and reactive
• Observe the EVD output (is it blocked?)

Control ICP by immediate measures:

• Open EVD to drain CSF
• Osmotherapy
  • Hypertonic saline to keep Na+ around 150
  • Consider intermittent mannitol
• Paralysis with cisatracurium

Exclude new intracranial pathology:

• CT brain

Maintain cerebral oxygen supply:

• Normoxia
• Normotension (CPP >60mmHg) - maintained with fluids or vasopressors
• Monitor cerebral oxygenation, keep the SjO2 >50%

Decrease cerebral oxygen demand:

• Sedate with propofol
• Ensure adequate analgesia

A CT brain is perfomed urgently. There is no new bleeding, but globally the cerebral oedema has worsened. ICP remains raised.

What options for controlling ICP would you consider?

The possible options include:

• Hypothermia
• Barbiturate coma
• Decompressive craniectomy

Exotic alternatives may include:

• THAM
• Dihydroergotamine
• Indomethacin

Historical alternatives had included 

• Steroids
• Hyperventilation

What is the evidence for decompressive craniectomy in TBI?

• The DECRA trial has demonstrated that long term outcome for traumatic brain injury patients is poorer with decompressive craniectomy.
  • No strong evidenc mortality benefit
  • Worse neurological outcome
• RESCUEICP trial (2016) demonstrated something similar:
  • Decompressive craniectomy was associated with lower mortality than medical management.
  • More survivors in the surgical group were dependent on others
  • Many criticisms: slow recruitment over 10 years with 50% of centres only recruiting 3 or fewer patients, 37% of patients in the medical group ended up having decompression anyway, etc.
• The new (2016) BTF Guidelines are careful to make clear that improving outcome is not what this technique is for. It is a measure to control otherwise uncontrollable ICP in situations, and it has some advantages.

What are the expected advantages of decompressive craniectomy in this scenario?

• Maybe some sort of mortality benefit (but this comes from cohort studies such as Sonuca et al, 2010)
• Shorter ICU stay
• Less ICP-targeting interventions
• Lower ICP

What are the complications of decompressive craniectomy?

• Brain hernation though the opening: This wil result in localised pressure necrosis around the edges, as well as venous "pinching" and congestion of the whole hernated mass. The smaller the craniectomy, the greater the risk of this occurring.
• Delayed paradoxical herneation: This is a weird complication of lumbar puncture in a pre-cranioplasty patient. Essentially, the opening of a lumbar drain allows the CSF to leak freely out of the spinal canal; however because the cranium is open, there is no negative pressure fastening the brainstem into the skull, and it readily herneates through the foramen magnum, killing the patient.
• Subdural hygroma: This is a collection of CSF which forms under the operative site after a craniectomy is finalised. It seems about half of all patients end up with this, to some degree. Most disappear harmlessly; some persist and cause a mass effect.

• Infection: The risk of this is abut 3-7%, with perioperative antibiotics. Bone flap osteomyelitis is more rare, but much more disturbing.
• Bleeding: A non-specific surgical complication.
• Post-traumatic hydrocephalus: In general, people who have decompressive craniectomy tend to develop this about 4 times as often as people who are managed non-surgicaly. However, people who end up needing decompression probably also had a more severe head injury. Potentially, some sort of arachnoid granulation injury could be the aetiological cause of this complication.
• Syndrome of the Trephined, or "Sinking Flap Syndrome": This is a long-term complication, associated with poor cognitive performance, memory loss, irritability, headaches and dizzyness. Nobody actually knows what causes it, but people tend to blame the fact that the brain is exposed to atmospheric pressure, and is thus subject to unusual changes of surface perfusion. These problems tend to resolve after cranioplasty.
• Bone resorption: After you have carefully positioned your bone flap and closed the patient's scalp, you may find to your dismay that within months the flap is gone. Where did it go? It was gobbled up by osteoclasts, as any stray piece of dead bone would be. Synthetic cranioplasty may be the answer to this problem, especially if the flap is in many pieces.